PMID- 32346039
OWN - NLM
STAT- MEDLINE
DCOM- 20201125
LR  - 20210428
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 10
IP  - 1
DP  - 2020 Apr 28
TI  - CB1 cannabinoid receptor-mediated plasticity of GABAergic synapses in the mouse 
      insular cortex.
PG  - 7187
LID - 10.1038/s41598-020-64236-5 [doi]
LID - 7187
AB  - The insular cortex plays pivotal roles in taste learning. As cellular mechanisms 
      of taste learning, long-term potentiation (LTP) at glutamatergic synapses is well 
      studied. However, little is known about long-term changes of synaptic efficacy at 
      GABAergic synapses in the insular cortex. Here, we examined the synaptic 
      mechanisms of long-term plasticity at GABAergic synapses in layer V pyramidal 
      neurons of the mouse insular cortex. In response to a prolonged high-frequency 
      stimulation (HFS), GABAergic synapses displayed endocannabinod (eCB)-mediated 
      long-term depression (LTD(GABA)). When cannabinoid 1 receptors (CB1Rs) were 
      blocked by a CB1R antagonist, the same stimuli caused LTP at GABAergic synapses 
      (LTP(GABA)) which was mediated by production of nitric oxide (NO) via activation 
      of NMDA receptors. Intriguingly, NO signaling was necessary for the induction of 
      LTD(GABA). In the presence of leptin which blocks CB1 signaling, the prolonged 
      HFS caused LTP(GABA) which was mediated by NO signaling. These results indicate 
      that long-term plasticity at GABAergic synapses in the insular cortex can be 
      modulated by combined effects of eCB and NO signaling. These forms of GABAergic 
      synaptic plasticity in the insular cortex may be crucial synaptic mechanisms in 
      taste learning.
FAU - Toyoda, Hiroki
AU  - Toyoda H
AD  - Department of Oral Physiology, Osaka University Graduate School of Dentistry, 
      Suita, Osaka, 565-0871, Japan. toyoda@dent.osaka-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200428
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (CNR1 protein, mouse)
RN  - 0 (Receptor, Cannabinoid, CB1)
RN  - 31C4KY9ESH (Nitric Oxide)
SB  - IM
MH  - Animals
MH  - Cerebral Cortex/*metabolism
MH  - GABAergic Neurons/*metabolism
MH  - *Long-Term Potentiation
MH  - Male
MH  - Mice
MH  - Nitric Oxide/metabolism
MH  - Receptor, Cannabinoid, CB1/antagonists & inhibitors/*metabolism
MH  - Signal Transduction
MH  - Synapses/*metabolism
PMC - PMC7189234
COIS- The authors declare no competing interests.
EDAT- 2020/04/30 06:00
MHDA- 2020/11/26 06:00
PMCR- 2020/04/28
CRDT- 2020/04/30 06:00
PHST- 2020/02/16 00:00 [received]
PHST- 2020/04/13 00:00 [accepted]
PHST- 2020/04/30 06:00 [entrez]
PHST- 2020/04/30 06:00 [pubmed]
PHST- 2020/11/26 06:00 [medline]
PHST- 2020/04/28 00:00 [pmc-release]
AID - 10.1038/s41598-020-64236-5 [pii]
AID - 64236 [pii]
AID - 10.1038/s41598-020-64236-5 [doi]
PST - epublish
SO  - Sci Rep. 2020 Apr 28;10(1):7187. doi: 10.1038/s41598-020-64236-5.